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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 16 patients suffering from cerebrovascular events, prostaglandin (PG) E2 was measured in their cerebrospinal fluid and correlated with their clinical status and evolution. Prostaglandin E2 ranged from 200-3000 pg (picogram)/ml of cerebrospinal fluid. A positive correlation was found between PG E2 levels and the severity and clinical outcome of the stroke.
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PMID:Measurement of prostaglandin E2 in cerebrospinal fluid in patients suffering from stroke. 59 74

In 10 normotensive healthy women between the 8th and 12th week of pregnancy complete cardiovascular studies were done before, during and after the intravenous administration of Prostaglandin E2 with the method of quantitative sphygmometry, unbloody measuring of the arterial blood pressure and direct electronical timing of the pulse wave velocity in the aorta. Prostaglandin E2 was infused with electric pump in the dosage of 0.65, 1.3 and 2.6 mug per minute for 30 minutes in each case. Arterial blood pressure and heart rate remains constant. Elasticity coefficient E' of the arteries and total peripheral resistance decreases, stroke volume, cardiac output, work and power of the heart increases significantly. These reactions of the cardiovascular system are much more pronounced than using Prostaglandin F2-alpha. Therefore prostaglandin E2 is characterized in relation to prostaglandin F2-alpha not only by a stronger uterine effectiveness, but also at the same time a pronounced influence on the cardiovascular system.
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PMID:[Cardiovascular effect of prostaglandin E 2 in early pregnancy]. 100 96

To test the efficacy of exogenous prostaglandins for vasodilator therapy in heart failure, we studied the hemodynamic, hormonal, and renal effects of prostaglandin E2 (1.5-150 ng/kg/min) in six conscious dogs before and after induction of heart failure by right ventricular pacing (250 beats/min, 10 days). In healthy dogs, PGE2 decreased the mean arterial pressure (MAP) by a reduction in total peripheral resistance (TPR), increased cardiac output (CO), stroke volume (SV), and heart rate with no effect on right atrial pressure (RAP). Plasma levels of renin (PRC) and norepinephrine (NE) were increased at the highest dosage. Renal plasma flow (RPF) and sodium excretion (UNaV) were augmented without a change in the glomerular filtration rate (GFR) and urine flow (UF). In dogs with heart failure, PGE2 lowered the MAP and TPR and elevated the CO and SV without an effect on the RAP, PRC, and NE. The RPF and GFR were not changed, but the increase in UNaV was preserved and UF significantly augmented. In experimental heart failure, PGE2 increases the CO due to arteriolar dilation and afterload reduction without inducing further neurohumoral activation and exerts potent natriuretic and diuretic action. Therefore, PGE2 may have beneficial effects in heart failure therapy.
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PMID:Prostaglandin E2 in dogs with heart failure: hemodynamic, hormonal, and renal effects. 128 Jul 9

Multiple elevation of the octanoic fatty acid level in human sera is often observed in some hepatic diseases which are accompanied by cardiovascular disorders, hypotension, and increased cardiac stroke volume. Different experiments reveal the hypotensive effect of octanoate. The present study investigates the octanoate action on the bioelectric and contractile activity of vascular smooth muscle tissues. Octanoate is shown to cause hyperpolarization of smooth muscle cells, reduction of spike potential frequency, and relaxation of vascular muscles. These effects are inhibited by indomethacin, which proves their prostaglandin nature. Octanoate action on stomach smooth muscle strips is inhibited by SC 19220, a specific competitive inhibitor of the contractile action of prostaglandins E2 and F2 alpha on the same tissues in vitro. Using thin-layer chromatography two PG fractions were isolated from arterial blood of octanoate treated rats and from a control group of rats. These fractions have identical chromatographic characteristics with those of PGE2 and PGF2 alpha. The level of the PG fraction with Rf value similar to that of PGE2 is significantly increased in octanoate treated animals while the other fraction tends to decrease.
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PMID:Effects of the medium chain octanoic fatty acid on the contractile activity of vascular smooth muscle tissues. 136 81

We examined whether the renal protective effect of the angiotensin I converting enzyme inhibitor enalapril in stroke-prone spontaneously hypertensive rats (SHRSP) is dose-related and associated with alterations in the urinary excretion of prostaglandin (PG) E2 and 6-keto-PGF1 alpha, a stable breakdown product of prostacyclin. Enalapril maleate at 1.5, 5 and 15 mg/kg/day or vehicle was chronically administered to saline-drinking SHRSP (six per group) starting at 8.1 weeks of age. Vehicle-treated SHRSP developed severe hypertension, proteinuria and strokes (age at death, 14 +/- 1 weeks; mean +/- S.E.). Enalapril prolonged survival dose-dependently and reduced proteinuria; all SHRSP given 15 mg/kg/day lived beyond 23 weeks of age without evidence of stroke or proteinuria. There was no effect of enalapril at any dose on systolic arterial blood pressure in spite of variable levels of urinary protein excretion and onset of stroke in the different groups. Likewise, urinary 6-keto-PGF1 alpha and PGE2 excretion did not differ among the groups except for an increase in 6-keto-PGF1 alpha in the 15 mg/kg/day group at one week after initiation of enalapril therapy. These results are consistent with a dose-related renal protective action of enalapril in saline-drinking SHRSP that is not closely associated with sustained alterations in urinary excretion of renal vasodilatory PGs.
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PMID:The antiproteinuric action of enalapril in stroke-prone spontaneously hypertensive rats is unrelated to alterations in urinary prostaglandins. 154 1

The goal of this study was to test the hypothesis that atherosclerosis alters responses of cerebral arteries and the ocular circulation to the activation in vivo of leukocytes and platelets. We measured blood flow to the brain and eye using microspheres and pressure in the cerebral microvessels of normal and atherosclerotic monkeys. The intracarotid injection of 10(-7) M N-formyl-L-methionyl-L-leucyl-L-phenylalanine to activate leukocytes did not alter cerebral blood flow in 11 normal or 10 atherosclerotic monkeys but increased the resistance of large cerebral arteries by 46 +/- 11% (mean +/- SEM) in the atherosclerotic animals. The injection of N-formyl-L-methionyl-L-leucyl-L-phenylalanine did not alter blood flow to the eye in 10 normal monkeys but decreased blood flow to the choroid by 38 +/- 9% in 11 atherosclerotic monkeys. The intracarotid injection of 3 x 10(-9) M prostaglandin E2, a leukocyte product, produced an increase in the resistance of large cerebral arteries in five atherosclerotic but not in six normal monkeys. Prostaglandin E2 reduced blood flow to the retina and choroid in the atherosclerotic monkeys by 62 +/- 22% and 65 +/- 17%, respectively. The intracarotid infusion of 25 micrograms/min collagen to activate platelets increased cerebral blood flow by 21 +/- 5% in 10 normal monkeys but did not alter it in 11 atherosclerotic monkeys. Collagen did not alter blood flow to the choroid in 10 normal monkeys but decreased it by 29 +/- 8% in 11 atherosclerotic monkeys.(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke 1991 Jun
PMID:Effect of atherosclerosis on cerebral vascular responses to activation of leukocytes and platelets in monkeys. 205 80

Prostaglandins (PG) E2,E1,6-keto-E1 and D2 at concentrations of 0.15-0.80 microM inhibited by 25% the generation of superoxide anions (O2-) in human polymorphonuclear leukocytes (PMNs) stimulated with formyl-methionyl-leucyl-phenylalanine (FMLP). The potency of that inhibition by either PGD2 or PGE1 was the same when zymosan was used as a stimulator whereas PGE2 and 6-keto-PGE1 were by 13 and 21 times less potent inhibitors of O2-) in zymosan-stimulated as compared to FMLP-activated PMNs. PGF2 alpha inhibited the generation of O2- by activated PMNs only when used at the highest concentration studied (30 microM). Prostacyclin, 6-keto-PGF1 alpha and Iloprost (a carbacyclin analogue of prostacyclin) at concentrations up to 30 microM showed no significant inhibition of O2- in human PMNs stimulated either with FMLP or with zymosan. It is concluded that PGD2 and PGEs use a common basic mechanism for inhibition of the generation of O2- by PMNs activated with FMLP or zymosan. PGD2 is most generously furnished with these properties. In addition to this basic mechanism PGE2 and 6-keto-PGE1 abrogate the FMLP-induced response by occupation of formyl peptide receptor of PMNs. It is hypothesised that inhibition of the generation of O2- in PMNs and, possibly, in other cells by PGD2, PGE2 and by products of prostacyclin biotransformation might be responsible for their cytoprotective action in myocardial infarction, stroke, liver damage and peripheral vascular disease.
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PMID:The effect of six prostaglandins, prostacyclin and iloprost on generation of superoxide anions by human polymorphonuclear leukocytes stimulated by zymosan or formyl-methionyl-leucyl-phenylalanine. 244 31

We explored the temporal and topographic relations between local cerebral blood flow and regional brain prostaglandin profile following prolonged or transient occlusion of the middle cerebral artery in cats. Each experimental group was subjected to a sham operation, prolonged ischemia, or recirculation. Local cerebral blood flow was measured by the hydrogen clearance method. Following in situ freezing, cortical samples were obtained from each gyrus for determination of prostaglandin (PG) F2 alpha, PGE2, 6-keto-PGF1 alpha, and thromboxane (TX) B2 concentrations by radioimmunoassay. During prolonged ischemia, the concentrations of PGF2 alpha and PGE2 within the middle cerebral artery territory were significantly increased. Immediately after recirculation, there was a prominent but transient increase in PGF2 alpha and PGE2 in gyri that had been exposed to moderate ischemia (perifocal area). By contrast, the increases in these prostaglandins were slow and less prominent in gyri that had been exposed to severe ischemia (the focal area). The concentration of 6-keto-PGF1 alpha did not change during prolonged ischemia but transiently increased following recirculation in both the focal and perifocal areas. The TXB2 concentration did not change in any experimental group. Our study revealed a homogeneous increase in the regional brain content of PGE2 or PGF2 alpha in spite of the heterogeneous reduction of local cerebral blood flow during prolonged ischemia. Following recirculation, the focal and perifocal areas exhibited different patterns of prostanoid content. No correlation was found between local cerebral blood flow and the regional concentration of any prostaglandin examined.
Stroke 1989 Jun
PMID:Prostaglandin profiles in relation to local circulatory changes following focal cerebral ischemia in cats. 272 49

Antihypertensive effect of enalapril (MK-421), an orally active non-sulfhydryl-containing converting enzyme inhibitor, was examined in stroke-prone spontaneously hypertensive (SHRSP) rats. The treatment was started at 14-15 weeks of age with tail blood pressure over 240 mmHg and was continued for 11 weeks. We used captopril as the reference drug. The dose of enalapril and captopril was 10 and 30 mg/kg per day, p.o., respectively. Enalapril showed a sustained antihypertensive effect from the 1st to the 11th week of the treatment. This antihypertensive effect was substantiated by the good increase in body weight; decrease in heart weight; decrease in incidences of vascular disease, nephrosclerosis, stroke and death. Enalapril treatment also prevented the increases in urine volume, and excretion of osmotically active solutes, Na, Cl and K with age. Captopril treatment showed about the same antihypertensive effect. No side effects were seen in the enalapril or captopril treated group. The antihypertensive potency of enalapril was about 3 times more than that of captopril. Enalapril and captopril slightly increased plasma renin concentration. Urinary excretion of PGE2 was not changed by enalapril or captopril treatment. These results clearly demonstrate the efficacy of long-term treatment with enalapril to prevent development of malignant hypertensive cardiovascular disease in SHRSP rats.
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PMID:Chronic effects of enalapril on blood pressure, stroke, plasma renin, urinary electrolytes and PGE2 excretion in stroke-prone spontaneously hypertensive rats. 299 88

Phospholipase A2 activity and prostaglandin synthesis were studied in the renal cortex and medulla of stroke-prone spontaneously hypertensive rats (SHRSP) and age-matched normotensive Wistar-Kyoto rats (WKY) aged 10-50 weeks. Enhanced phospholipase A2 activity was found in both the cortical and the medullary microsomes of SHRSP kidneys. Phospholipase A2 activity progressively increased with age in SHRSP, but not in WKY. Prostaglandin E2 (PGE2) and thromboxane A2 (TXA2) were the major prostaglandins found in the cortex, and PGE2 was the major prostaglandin found in the medulla. Prostaglandin l2 (PGI2) was synthesized in both the cortex and medulla, but cortical PGI2 synthesis was much lower than medullary synthesis. Enzymatic activity for all prostaglandin syntheses analysed here were higher in SHRSP. There was a greater age-related increase in prostaglandin synthesis in SHRSP kidneys than in WKY kidneys. In addition, the ratios of PGE2/TXB2 and 6-keto-prostaglandin F1 alpha (PGF1 alpha)/thromboxane B2 (TXB2) decreased in SHRSP. This may produce vasoconstriction and increase vascular resistance in SHRSP. These data suggest that increased prostaglandin synthesis and phospholipase A2 activity have an important role in the development and maintenance of hypertension in SHRSP.
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PMID:Renal prostaglandins and phospholipase A2 in spontaneously hypertensive rats. 330 39


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